F. G. Cunningham

Peripartum heart failure: Idiopathic cardiomyopathy or compounding cardiovascular events?

During a 12-year period, when more than 106,000 women were delivered, 28 women with peripartum heart failure of obscure etiology that initially was diagnosed as peripartum cardiomyopathy were studied. None had obvious underlying cardiac disease or iatrogenic fluid overload, and in all an assiduous search for underlying cardiovascular disease was launched. In 21 of these 28 women, heart failure was attributed to chronic underlying disease (chronic hypertension in 14, forme fruste mitral stenosis in four, and morbid obesity in one) or viral myocarditis. Importantly, these women also had multiple compounding cardiovascular factors--preeclampsia, cesarean section, anemia, and infection--which, when superimposed on those of pregnancy, acted in concert to cause heart failure. In seven women, the cause for cardiomegaly and global hypokinesis was not found, and peripartum cardiomyopathy was diagnosed. Compared with women with explicable causes of peripartum heart failure, these women did poorly: six had persistent cardiomegaly and heart failure, and four of these died within four months to eight years. From these observations, the authors conclude that idiopathic peripartum cardiomyopathy is uncommon, and that in most women with peripartum heart failure of obscure etiology, underlying chronic disease will be identified. Heart failure in these women ensues when the cardiovascular demands of normal pregnancy are amplified further by common pregnancy complications superimposed upon these underlying conditions that cause compensated ventricular hypertrophy.

Thyrotoxicosis complicating pregnancy

During the 12-year period from 1974 through 1985, nearly 120,000 women were delivered of infants at Parkland Hospital, and pregnancy was complicated by overt thyrotoxicosis in 60 of them (1:2000). Initial treatment was based on clinical assessment, and propylthiouracil was usually given in doses of 300 to 800 mg daily. In compliant women seen by midpregnancy, euthyroidism was achieved by a mean of 8 weeks; however, the daily dose was decreased to less than or equal to 150 mg by delivery in only 10%. Metabolic status at delivery correlated directly with pregnancy outcome, and women treated earlier in pregnancy were more likely to be euthyroid at delivery and to have good outcomes. Diagnosis of thyrotoxicosis antecedent to pregnancy was associated with earlier treatment, and 80% of 28 such women were euthyroid by delivery. Conversely, 32 women with a first diagnosis during pregnancy had the preponderance of morbidity, including five of six stillbirths and six of seven cases of heart failure. This group was characterized by a relative delay in gestational age at diagnosis. Preterm delivery, perinatal mortality, and maternal heart failure were more common in women who remained thyrotoxic despite treatment and in those who were never treated. Although we infrequently achieved maintenance doses recommended by most, because there were minimal adverse effects from therapy described here and because uncontrolled thyrotoxicosis caused significant maternal and perinatal morbidity, aggressive medical therapy seems appropriate, especially when pregnancy is advanced.

Mechanisms of hemolysis and anemia associated with acute antepartum pyelonephritis

Anemia develops in about a fourth of women whose pregnancy is complicated by pyelonephritis, although its exact mechanism has not been defined clearly. In this study of 18 women with antepartum pyelonephritis, although only a third had anemia (hematocrit less than 30 vol/dl), there was evidence for hemolysis in all 18. Specifically there was a mean decrease in hematocrit of 5 vol/dl from admission to discharge. With scanning electron microscopy, we compared erythrocyte morphologic aberrations that were found in women with renal infection with those of normally pregnant women, and the former had significantly increased proportions of echinocytes in particular, but schistocytes and spherocytes were increased also (total 10.3% vs 1.4%, p less than 0.0001). These changes, especially echinocytosis, have been induced in vitro by lipopolysaccharide, and they are known to lead to premature red blood cell destruction in vivo. We conclude that hemolysis with subsequent anemia in pregnant women with pyelonephritis is caused by lipopolysaccharide-induced red blood cell membrane damage.

Chronic renal disease and pregnancy outcome

non-significantly higher occurrence of pre-eclampsia among grand-daughters than in grand-daughters-in-law. No difference was seen by whether grand-daughters descended through sons or daughters. With increasing numbers of affected daughters or grand-daughters the probability rose of finding more affected women in a family. Hypotheses of single recessive and dominant gene inheritance were compared and maximum likelihood estimates for gene frequency obtained. For a single recessive gene model this was 0.31 reflecting a population prevalence of 9.6%. whereas a dominant model with incomplete penetrance gave 0. I4 at 48% gene penetrance, corresponding to a population prevalence of 0.9% homozygous expression of severe disease and I I% heterozygous expression of milder disease. Either genetic model could tit the data.

Pulmonary injury complicating antepartum pyelonephritis

Over a 7-year period, 15 pregnant women admitted to Parkland Memorial Hospital for acute pyelonephritis developed respiratory insufficiency characterized by dyspnea, tachypnea, hypoxemia, and radiographic evidence of pulmonary infiltrates. Clinical manifestations usually appeared 24 to 48 hours after the patient was admitted and varied from mild respiratory distress to pulmonary failure in three; these three required tracheal intubation and mechanical ventilation. We found no evidence that pulmonary edema was caused by intravenous fluid overload. Oxygen therapy and ventilation were given to maintain the arterial PO2 at 80 mm Hg or greater, and erythrocyte transfusions were given to six women to correct anemia. Women with pulmonary injury were more likely to have multisystem derangement than a control group without respiratory involvement, but there were no clinical risk factors that were predictive at admission. This syndrome was probably caused by permeability pulmonary edema, likely mediated by endotoxin-induced alveolar-capillary membrane injury since other evidence of endotoxemia was common. Thrombocytopenia, hemolysis, intravascular coagulation, renal dysfunction, and transient cardiomegaly concomitant with hyperdynamic ventricular function are all explicable from endotoxin effects.